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Objectives
Propofol-based total intravenous anesthesia (TIVA) has been used successfully for liver transplantation (LT) in recent years. However, there are few discourses in the literature which focus on the merits and weakness in perioperative management, biochemical changes, and postoperative recovery between TIVA and desflurane anesthesia (DES).
Methods
We retrospectively compared the circumstances of liver transplantation recipients who had the surgery carried out under propofol-based TIVA or DES in the period from September 2007 to August 2010. Preoperative characteristics, date of intraoperative management, hemodynamic profiles, concentration of anesthetics, biochemical changes, and circumstances of postoperative recovery were retrieved from the hospital database for analysis.
Results
We included 111 patients who received the surgery under either TIVA (n = 66) or DES (n = 45). Patient demographics, baseline laboratory data, operation time, and fluid management did not differ between the two groups. In comparison with the DES group, fewer patients had to be administered norepinephrine (21.2% vs. 42.2%; p = 0.020) in the TIVA group; moreover, the total dosage of norepinephrine was lower (0.003 ± 0.005 mg vs. 0.006 ± 0.008 mg; p = 0.012) in the TIVA group during liver reperfusion phase. Blood lactate level was higher in the DES group than in the TIVA group after the anhepatic phase. TIVA patients woke up faster than those in the DES group (54.0 ± 33.4 minutes vs. 95.0 ± 78.3 minutes; p = 0.034).
Conclusion
Our results suggest that propofol-based TIVA may provide better hemodynamics and microcirculation during the anhepatic phase in liver transplantation.

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As known, long-term morphine infusion leads to tolerance. We previously demonstrated that both co-infusion and post-administration of ultra-low dose (±)-naloxone restores the antinociceptive effect of morphine in morphine-tolerant rats. However, whether the mechanism of the action of ultra-low dose (±)-naloxone is through opioid receptors or not. Therefore, in the present study, we further investigated the effect of ultra-low dose (+)-naloxone, it does not bind to opioid receptors, on the antinociceptive effect of morphine.
Male Wistar rats were implanted with one or two intrathecal (i.t.) catheters; one catheter was connected to a mini-osmotic pump, used for morphine (15 μg/h), ultra-low dose (+)-naloxone (15 pg/h), morphine plus ultra-low dose (+)-naloxone (15 pg/h) or saline (1 μl/h) infusion for 5 days. On day 5, either ultra-low dose (+)-naloxone (15 pg) or saline (5 μl) was injected via the other catheter immediately after discontinued morphine or saline infusion. Three hours later, morphine (15 μg in 5 μl saline) or saline were given intrathecally. All rats received nociceptive tail-flick test every 30 min for 120 min after morphine challenge at different temperature (45∼52 °C, respective).
Our results showed that, both co-infusion and post-treatment of ultra-low dose (+)-naloxone with morphine preserves the antinociceptive effect of morphine. Moreover, in the post administration rats, ultra-low dose (+)-naloxone further enhances the antinociceptive effect of morphine.
This study provides an evidence for ultra-low dose (+)-naloxone as a therapeutic adjuvant for patients who need long-term opioid administration for pain management.

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Object Baicalein has been shown to offer neuroprotection in the ischemic brain, but its effect in subarachnoid hemorrhage (SAH) is unknown. The authors used a double-hemorrhage model to study the role of early baicalein treatment in SAH. Methods Subarachnoid hemorrhage was induced in male Wistar rats through a repeat injection of autologous blood at a 48-hour interval. Rats subjected or not subjected to SAH received a 30-mg/kg baicalein injection 3 hours after SAH and daily for 6 consecutive days, and results were compared with those obtained in vehicle-treated control rats. Mortality of the rats was recorded. Neurological outcome was assessed daily. Cerebrospinal fluid dialysates were collected and examined for glutamate concentrations. Cerebral vasospasm (CVS), brain water content, neuron variability, expression of glutamate transporter-1 (GLT-1), immunoreactivity of astrocyte, and level of malondialdehyde, activities of superoxide dismutase (SOD), and catalase in brain tissues content were determined on post-SAH Day 7. Results Mortality rate, neuronal degeneration, brain water content, and CVS were decreased and neurological function improved in the baicalein-treated rats. Baicalein increased astrocyte activity and preserved GLT-1, which attenuated the glutamate surge after SAH. Baicalein also provided antioxidative stress by preserving activities of SOD and catalase and decreased malondialdehydelevel after SAH. The glutamate, body weight, neurological scores, and glial fibrillary acidic protein activity were significantly correlated. The CVS was correlated with neuronal degeneration, and GLT-1 was correlated with oxidative stress. Conclusions Early baicalein treatment attenuated CVS and limited neurological injury following SAH. These data may indicate clinical utility for baicalein as an adjunct therapy to reduce brain injury and improve patient outcomes.

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A tourniquet is commonly used in limb surgery. Tourniquet inflation after a period of time may produce painful sensation. While the mechanisms of tourniquet-induced pain are still unknown, two components, pressure and ischemia, have been proposed. In this study, in vivo microdialysis was used to detect changes in intrathecal glutamate, an excitatory amino acid highly relevant to pain transmission, following hindlimb tourniquet application and femoral artery occlusion in the rat.
Male Wistar rats were used. For the tourniquet study, 6 rats of the study group received 30 minutes right hindlimb tourniquet inflation and another 6 rats as the control group received only tourniquet application without inflation. In the femoral artery occlusion study, 6 rats of the study group received 30 minutes right femoral artery occlusion and another 6 rats as the control group received only sham operation without femoral artery occlusion. Cerebrospinal fluid dialysates were collected prior to, during, and after tourniquet application or femoral artery occlusion. Glutamate was measured by HPLC.
A significant increase in intrathecal glutamate release was found during the tourniquet inflation period, and it returned to baseline after tourniquet deflation. No change of glutamate release was noted during femoral artery occlusion or after femoral artery reperfusion.
The intrathecal glutamate release was increased by the hindlimb tourniquet inflation, but not influenced by femoral artery occlusion in the rat.

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The purpose of this preliminary study was to examine whether collateral meridian (CM) therapy was feasible in treating knee osteoarthritis (OA) pain.
Twenty-eight patients with knee OA and knee pain were randomly allocated to 2 groups. The CM group patients received CM therapy, whereas the control patients received placebo treatment for knee pain relief. Patients in the CM group received 2 CM treatments weekly for 3 weeks. The outcome measures were pain intensity on a visual analog scale, and knee function was determined using the Western Ontario and McMaster Universities Osteoarthritis Index.
In the CM group, the posttreatment visual analog scale and Western Ontario and McMaster Universities Osteoarthritis Index scores were lower than those of the control group; a significant reduction in pain intensity (P = .02, P = .01, respectively) and improvement in knee function (P = .04, P = .03, respectively) were shown in the CM group at the second and third week.
Collateral meridian therapy may be feasible and effective for knee OA pain relief and knee function recovery. Therefore, additional randomized control trials are warranted.

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The tricyclic antidepressant amitriptyline binds with high affinity to N-methyl-d-aspartate receptors (NMDARs) and inhibits NMDAR-mediated events. Activation of the postsynaptic density protein-95 (PSD-95)/NMDAR-mediated downstream signaling cascade, including neuronal nitric oxide synthase (nNOS) and protein kinase gamma (PKCγ), has been shown to be involved in morphine tolerance. The present study examined the potential effect of amitriptyline on chronic morphine infusion-induced spinal PSD-95/NMDAR/nNOS/PKCγ signaling in morphine tolerance. Male Wistar rats were implanted with an intrathecal catheter and received an intrathecal infusion of saline or amitriptyline (15 μg/h), morphine+saline (tolerance induction, 15 μg/h), or morphine+amitriptyline for 5 days. Co-administration of amitriptyline with morphine not only preserved the antinociceptive effect of morphine, but also attenuated astrocyte activation in the rat spinal cord dorsal horn. On day 5 after drug infusion, increased expression and phosphorylation of spinal membrane NMDAR NR1 subunit and expression of PSD-95 were observed following chronic morphine infusion and these effects were attenuated by amitriptyline co-infusion. Upregulation of NMDAR-induced intracellular nNOS expression was also inhibited by amitriptyline co-infusion in chronic morphine-infused rats. Furthermore, amitriptyline co-infusion significantly inhibited morphine-induced PKCγ expression in both the cytosol and membrane of spinal neurons. These findings suggest that the attenuation of morphine tolerance caused by amitriptyline is due to downregulation of NMDAR NR1 subunit expression in the synaptosomal membrane accompanied by decreased expression of the scaffolding protein PSD-95. The effects of amitriptyline in attenuating astrocyte activation and reversing tolerance to morphine may be due, at least in part, to inhibition of the PSD-95/NMDAR NR1/nNOS/PKCγ signaling cascade.

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Patent blue (PB) dye has been successfully used worldwide in breast and cervix surgeries with few complications. Interference of oxyhemoglobin saturation reading by pulse oximetry (SpO(2)) and methemoglobinemia, from injection of PB dye, have rarely been reported in breast and cervix surgeries. We report here the first case of interference of SpO(2) reading, advent of methemoglobinemia, and blue urine from the use of PB dye, which occurred concurrently in a female undergoing bilateral modified radical mastectomy. The unexpected events might be a consequence of excessive administration of PB dye. We also reviewed the published discourses in literature on the adverse effects of PB dye.

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Cough causes poor quality of emergence from anesthesia and risks of several complications. We compared fentanyl and an antitussive action of tramadol on the quality of emergence and postoperative outcome.
A total of 110 adults (18 to 83 y) of American Society of Anesthesiologists physical status I-III undergoing elective lumbar microdiscectomy with intubated total intravenous anesthesia were randomly divided into 2 groups of 55 each. The patients assigned to the fentanyl group received a dose of 1 μg/kg of fentanyl, whereas those assigned to the tramadol group received 1 mg/kg of tramadol, at the beginning of skin closure. We recorded the incidence of cough, quality of extubation at fixed times, maximal heart rates, maximal blood pressure during emergence, postoperative pain scores, and consumption of fentanyl. In addition, postoperative sore throat (POST), hoarseness, postoperative nausea and vomiting, and other anesthetic and surgical-related complications were recorded.
Tramadol reduced cough incidence, improved extubation quality, and provided more stable hemodynamics during emergence. There was no significant difference in postoperative pain, fentanyl consumption, incidence and severity of POST, hoarseness, and postoperative nausea and vomiting between groups. Moreover, we found that the incidence of POST did not correlate with cough incidence.
A dose of 1 mg/kg of tramadol administered intravenously 30 minutes before the expected extubation, compared with 1 μg/kg of fentanyl, decreased cough incidence, improved emergence quality, and provided stable hemodynamics. However, there was no significant difference between tramadol and fentanyl in pain scores and fentanyl consumption postoperatively.

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Local anesthetic-induced neurotoxicity is one of the potential causes of postspinal anesthesia neurologic injury. Many experimental and clinical studies have demonstrated that lidocaine is more neurotoxic than bupivacaine. The mechanisms of local anesthetic-induced neurotoxicity remain unclear. Glutamate is an excitatory amino acid and widely exists in the central nervous system. Overstimulation of the glutamate receptors may produce neuronal toxic effect. In this study, we used in vivo microdialysis to examine the glutamate release in cerebrospinal fluid (CSF) after intrathecal lidocaine and bupivacaine injection.
Male Wistar rats were used. Administration of lidocaine (5 groups: normal saline, 2.5%, 5%, 10%, and 10% + MK-801 intrathecally injected) and bupivacaine (4 groups: normal saline, 0.25%, 0.5%, and 1% intrathecally injected) was performed in both microdialysis and postinjection neurologic sequelae studies. After intrathecal injection of the studied agents, the CSF dialysates were collected in 10-minute intervals for 2 hours. Cerebrospinal fluid glutamate concentrations were measured by high-performance liquid chromatography. In addition, tail-flick latencies were examined daily before and after microdialysis for 4 days.
Intrathecal lidocaine concentration-dependently elevated glutamate release in CSF. Pretreatment with MK-801 significantly inhibited the glutamate release induced by 10% lidocaine. Intrathecal bupivacaine has no influence on glutamate release in CSF. The tail-flick latencies were significantly prolonged for 4 days after intrathecal lidocaine injection, and these effects were in a concentration-dependent manner. Pretreatment with MK-801 significantly reversed the 10% lidocaine-induced prolonged tail-flick latencies. There was no difference of the tail-flick latencies among the bupivacaine-treated groups.
Intrathecal lidocaine caused a concentration-dependent increase of the CSF glutamate release and postinjection neurologic impairment; these effects can be reversed by MK-801. However, intrathecal bupivacaine shows no influence. We suggest that glutamate may be involved in the pathogenesis of lidocaine-induced spinal neurotoxicity.

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Chronic opioid therapy induces tolerance and hyperalgesia, which hinders the efficacy of opioid treatment. Previous studies have shown that inhibition of neuroinflammation and glutamatergic receptor activation prevents the development of morphine tolerance. The aim of the present study was to examine whether N-Methyl-D-aspartate receptors are involved in the regulation of chronic morphine-induced neuroinflammation in morphine-tolerant rats. Morphine tolerance was induced in male Wistar rats by intrathecal infusion of morphine (15 μg/h) for 5 days. Tail-flick latency was measured to estimate the antinociceptive effect of morphine. Morphine challenge (15 μg, intrathecally) on day 5 at 3h after discontinuation of morphine infusion produced a significant antinociceptive effect in saline-infused rats, but not in morphine-tolerant rats. Pretreatment with MK-801 (20 μg, intrathecally) 30 min before morphine challenge preserved its antinociceptive effect in morphine-tolerant rats. Morphine-tolerant rats expressed high levels of the pro-inflammatory cytokines interleukin-1β, interleukin-6, and tumor necrosis factor-α and the increase in interleukin-1β and interleukin-6, and tumor necrosis factor-α levels was prevented by MK-801 pre-treatment at both the protein and mRNA levels. The results show that a single dose of MK-801 reduces the increase in pro-inflammatory cytokines in the spinal cord, thus re-sensitizing neurons to the antinociceptive effect of morphine in morphine-tolerant rats. This study provides a piece of theoretical evidence that NMDA antagonist can be a therapeutic adjuvant in treating morphine tolerant patients for pain relief.

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Glutamate and glutamate transporters (GTs) (including glutamate/aspartate transporter, glutamate transporter-1, and excitatory amino acid carrier 1) have important roles in the pathogenesis of ischemic neurological injury. The changes in glutamate, GTs, and neuronal injury after subarachnoid hemorrhage (SAH) have not been widely investigated. In this study, we examined the changes in extracellular glutamate concentration, GTs, wall thickness of basilar arteries (BAs), and neuronal degeneration in experimental SAH rats.
An intrathecal microdialysis probe was inserted into male Sprague Dawley rats. SAH was induced using a double-hemorrhage model. To measure glutamate concentrations, extracellular dialysates were collected for 30 minutes before, and daily for 7 days after SAH. Changes in neurological scores, body weight, and BA wall thickness were measured. The neuron degeneration in the hippocampus and the changes of GTs in the cerebral cortex and hippocampus were measured.
Glutamate concentrations were significantly higher in SAH rats from day (D)1 to D7 after SAH compared with the sham rats, especially at D1. A significant body weight reduction and neurological defects were observed at D3 after SAH. The walls of BAs in SAH rats were significantly thicker compared with those of sham rats; the maximum change was observed at D7. Hippocampal neuronal degeneration was observed after SAH and the highest severity was at D7. The expression of GTs was downregulated after SAH and persisted for 7 days.
SAH induced in the double-hemorrhage rat model may produce an excessive and prolonged increase of extracellular glutamate concentrations and downregulation of GTs, which are accompanied by BA wall thickness, and hippocampal neuronal degeneration.

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We investigated the analgesic efficacy of bilateral superficial cervical plexus block in patients undergoing thyroidectomy and to determine whether it reduces the adverse effects of general anesthesia.
We prospectively recruited 162 patients who underwent elective thyroid operations from March 2006 to October 2007. They were randomly assigned to receive a bilateral superficial cervical block (12 ml per side) with isotonic saline (group A; n = 56), bupivacaine 0.5% (group B; n = 52), or levobupivacaine 0.5% (group C; n = 54) after induction of general anesthesia. The analgesic efficacy of the block was assessed with: intraoperative anesthetics (desflurane), numbers of patients needing postoperative analgesics, the time to the first analgesics required, and pain intensity by visual analog scale (VAS). Postoperative nausea and vomiting (PONV) for 24 h were also assessed by the "PONV grade." We also compared hospital stay, operative time, and discomfort in swallowing.
There were no significant differences in patient characteristics. Each average end-tidal desflurane concentration was 5.8, 3.9, and 3.8% in groups A, B, and C, respectively (p < 0.001). Fewer patients in groups B and C required analgesics (A: B: C = 33:8:7; p < 0.001), and it took longer before the first analgesic dose was needed postoperatively (group A: B: C = 82.1:360.8:410.1 min; p < 0.001). Postoperative pain VAS were lower in groups B and C for the first 24 h postoperatively (p < 0.001). Incidences of overall and severe PONV were lower, however, there were not sufficient numbers of patients to detect differences in PONV among the three groups. Hospital stay was shorter in group B and group C (p = 0.011). There was no significant difference in operative time and postoperative swallowing pain among the three groups.
Bilateral superficial cervical plexus block reduces general anesthetics required during thyroidectomy. It also significantly lowers the severity of postoperative pain during the first 24 h and shortens the hospital stay.

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Naloxone is commonly used to reverse narcotic intoxication. However, its use is not entirely free of hazards. For instance, pulmonary edema (PE) has been reported to arise with the mechanism of over-sympathetic discharge caused by release of cat-echolamine or central neurogenetic responses to narcotic reversal. Here, we report a healthy young patient who, after undergoing an uneventful uvulopalatopharyngo-plasty for obstructive sleep apnea hypopnea syndrome, developed PE following administration of naloxone. Fentanyl-induced respiratory depression was found during anesthesia emergence and thus naloxone was indicated for reversal. Unfortunately, upper airway obstruction-induced negative pressure PE occurred following naloxone administration. From this case, we suggest that a patent airway should be ascertained before naloxone administration for treating narcotic-induced respiratory depression.

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Peripheral deafferentation induced by neuraxial anesthesia reduces the degree of cortical arousal. This study investigated whether epidural analgesia blockade decreased sedation, as measured by the rapidly extracted auditory evoked potentials index, A-line autoregressive index (AAI) and Ramsay Sedation Scale (RSS) in sedated surgical intensive care patients, and looked at whether this was a concentration-dependent effect of lidocaine.
Forty patients underwent major lower abdominal surgery and received epidural analgesia in the surgical intensive care unit. Patients were continuously sedated with propofol to achieve an RSS value of 3, randomly divided into two groups, and received epidural analgesia with 10 mL of 0.5% or 1% lidocaine. Sedation was evaluated using the RSS and AAI, and analgesia was evaluated using a visual analog scale (VAS). RSS, AAI, electromyography (EMG) activity of AAI and VAS values were recorded at 5 minutes before and 30, 60 and 90 minutes after epidural lidocaine administration.
Epidural 0.5% lidocaine produced a reduction of AAI, EMG and VAS at 30, 60 and 90 minutes after administration. For 1% epidural lidocaine administration, AAI, EMG and VAS were also reduced at 30, 60 and 90 minutes after epidural lidocaine administration. However, there was no difference in the AAI between the two concentrations; moreover, no significant change was observed in the RSS.
Epidural lidocaine analgesia could potentiate sedation in patients evaluated by the AAI, but had no effect on the RSS. The present study suggests that the AAI could provide an objective and more precise index than the RSS in evaluation of sedation level in patients who are undergoing epidural pain management in the intensive care unit.

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The pathophysiology of complex regional pain syndrome type 1 (CRPS 1) correlates with variances in both the peripheral and central nerve system. We attempted to explore the topographic correlation between changes in regional cerebral blood flow (rCBF) and 3-phase bone scans during treatments of a series of somatic nerve blocks.
The case we present here is a 24-year-old man, who suffered CRPS 1 in his right upper extremity for 4 months, and conservative therapy proved to be ineffectual to him. As he did not respond to stellate ganglion block, the syndrome was regarded as sympathetically independent pain (SIP). However, after administering a series of brachial plexus block and local anesthetics, complete resolution of pain, and restoration of function were manifested. In addition, an increase in rCBF, evidenced by single-photon emission computed tomography (SPECT), and changes in the 3 phase bone scan before and after the nerve block appear to correlate well with the clinical improvement.
The changes in rCBF seem to support the theory that the pathogenesis of CRPS is also related to the central nervous system. Multiple somatic nerve blocks (SNB) not only improved physical function but also reversed the CRPS symptoms, for which we presume that reduced nociceptive input signals led to cortical reorganization.

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When administering postoperative acute pain services, particularly regarding patient- controlled epidural analgesia, difficulties may occasionally be encountered during removal of the epidural catheter. In this report, we present an instance of difficult removal of epidural catheter in a female patient undergoing open reduction and internal fixation of the femoral neck with patient-controlled epidural analgesia as the means of postoperative pain control. The patient had satisfactory analgesia for 3 days; however, during the removal of the epidural catheter, difficulties were encountered and epidurogram revealed that the epidural catheter had become anchored in the anterior epidural space without kinking or knotting. Subsequently, the patient was requested to lie prone on the surgical table with a pillow placed beneath her lower abdomen and catheter removal was tried again. Fortunately, the epidural catheter was removed easily without the need for a guided stylet. We believe that the cause of the difficult removal of the epidural catheter in this case might have resulted from an unusual and unwanted deeper anchorage of the catheter along the anterior epidural space during placement. We also include some discussion on the management of problematic removal.

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Postoperative sore throat (POST) is a common complication after endotracheal intubation. We compared the effectiveness on POST of spraying the endotracheal tube (ETT) cuff with benzydamine hydrochloride, 10% lidocaine, and 2% lidocaine.
Three hundred seventy-two patients were randomly allocated into 4 groups. The ETT cuffs in each group were sprayed with benzydamine hydrochloride, 10% lidocaine hydrochloride, 2% lidocaine hydrochloride, or normal saline before endotracheal intubation. After insertion, the cuffs were inflated to an airway leak pressure of 20 cm H(2)O. Anesthesia was maintained with propofol. The patients were examined for sore throat (none, mild, moderate, or severe) at 1, 6, 12, and 24 hours after extubation.
The highest incidence of POST occurred at 6 hours after extubation in all groups. There was a significantly lower incidence of POST in the benzydamine group than 10% lidocaine, 2% lidocaine, and normal saline groups (P < 0.05) at each observation time point. At 6 hours after extubation, the incidence of POST was significantly lower in the benzydamine group (17.0%) compared with 10% lidocaine (53.7%), 2% lidocaine (37.0%), and normal saline (40.8%) groups (P < 0.05). The benzydamine group had significantly decreased severity of POST compared with the 10% lidocaine, 2% lidocaine, and normal saline groups (P < 0.05) at each observation time point. Compared with the 2% lidocaine and normal saline groups, the 10% lidocaine group had significantly increased severity of POST at 1, 6, and 12 hours after extubation. There were no significant differences among groups in local or systemic side effects.
Spraying benzydamine hydrochloride on the ETT cuff is a simple and effective method to reduce the incidence and severity of POST.